Human Energy Metabolism Research Articles

Consumption of Coffee Polyphenols Increases Fat Utilization in Humans

Long-term ingestion of coffee polyphenols (CPP) reduces body fat in humans. The aim of the present study was to investigate the effect of daily consumption of CPP on energy metabolism in humans. Seven healthy male subjects, with a mean (±SEM) age of 34.7±2.0 y and a body mass index (kg/m2) of 21.8±0.6, participated in a placebo-controlled, double-blind, crossover intervention study with two different test beverages. The subjects consumed 185 g of a test beverage with or without CPP (359 mg) daily for 1 week. Energy metabolism was evaluated by indirect calorimetry before and after the test period after fasting and up to 3.5 hr postprandially, and during cycle ergometry. Indirect calorimetry showed that, compared to 1-week ingestion of the control beverage, 1-week ingestion of the CPP beverage led to significantly higher oxygen consumption in the sedentary period and during the cycle ergometry. CPP beverage consumption led to a higher fat utilization in the sedentary period and a higher anaerobic threshold during exercise compared with control beverage consumption. In conclusion, daily consumption of CPP increases postprandial fat utilization in healthy humans.

Energy Expenditure: Measurement of Human Metabolism

Obesity is one of the most prevalent chronic diseases globally, especially in the United States. While the United States gained an early lead in unnecessary weight gain, most other countries are quickly closing the gap. The latest U.S. National Health and Nutrition Examination Survey (NHANES, http://www.cdc.gov/nchs/nhanes.htm) documents that about one third of adults in the United States are now overweight [a body-mass index (BMI) between 25 and 30 kg/m2] and another one third (61 million) are considered obese (BMI >30 kg/m2). Being obese is a strong risk factor for cardiovascular diseases, type 2 diabetes, osteoporosis, some cancers, and depression. The economic impact of this condition is staggering: in 2008, more than 147 billion dollars were spent just in the United States for medical costs related to obesity. Time lost from work and spending on weight loss costs even more.

Investigation of the Lipid Metabolism during Drosophila Larva Development by Coherent Anti-Stokes Raman Scattering (CARS) Microscopy

Drosophila melanogaster is one of the most valuable model organisms in studying genetics and developmental biology. The Drosophila fat body stores lipids that act as an energy source for the developing animal during its larval stages. Studies on lipid metabolism of the fat body allow us to better understand human energy metabolism and related illnesses.Coherent anti-Stokes Raman Scattering (CARS) microscopy is a nonlinear optical (NLO) technique which gives three-dimensional imaging based on chemically-selective vibrational scattering signals without any labeling agent. It has been widely used in the imaging of lipids in biological samples due to the strong CARS signal from carbon-hydrogen (C-H) bonds. Here we used CARS microscopy to image the distribution of the fat body in Drosophila larva in vivo with minimal invasion. Combined with two-photon excitation (TPE) and second harmonic generation (SHG), we could also obtain images of internal organs from autofluorescence and collagen/muscular tissues from SHG simultaneously in the same NLO platform. This study allowed us to visualize the three-dimensional structures of the Drosophila larva under the most natural living condition which cannot be achieved by conventional biochemical staining and labeling system. We further investigated the development of the fat body during different larval stages and under various conditions through long-term in vivo observations.To our knowledge, this is the first demonstration on in vivo imaging of unstained/label-free Drosophila fat body to get new insights into the lipid metabolism during Drosophila larva development by using multimodal NLO microscopy.

The supply chain of the brain – An economic approach to human energy metabolism

Event Abstract Back to Event The supply chain of the brain – An economic approach to human energy metabolism Dirk Langemann1* 1 Technische Universität Braunschweig, Institute of Computational Mathematics, Germany The description of the human metabolism from the food intake to the energy consumption in the body periphery and in the brain includes a tremendous number of regulatory pathways and involved substances. The abstraction from energy supporting and transporting substances to energy contents in selected compartments and the summarization of redundant regulatory pathways leads to integrated models of the metabolism. It is the clarity of these models, which allows us to develop a systemic understanding of the human metabolism as a whole by mathematical methods, in particular by the theory of dynamical systems. The named integrated models are supply chains, which are well-discussed in economics and logistics. In analogy to the systemic investigation of the metabolism, the economical mechanisms are not completely quantified although their basic directions of regulation are without any doubt. Nevertheless, worthwhile qualitative explanations are derived. Following this approach, the metabolism is regarded as an energy supply chain from the food intake to the final energy consumers in the organism. The complex and not completely quantified regulatory mechanisms are abstracted to their pull and push components, which mathematically speaking corresponds to a linearization. The pull component of a flux is the part regulated by the receiver, the push component is the part governed by the supplier. Robust modeling techniques assure the conservation of the qualitative behavior of the dynamical systems. The simple distinction between pull and push component yields qualitative properties of the considered dynamical system. Economic supply chains as well as metabolic supply chains with dominating pull component show a retrograde propagation of perturbation. Hence, effects of perturbations are found in front of their causes with respect to the transport direction. This implies that the cause of an obese body is behind the body compartment in the supply chain. Consequently, the Selfish-brain theory assumes the cause to be located in the brain. Integrated models are used to support such assumptions, e.g. the observation of a circadian rhythm of food intake requires the existence of a relevant energy consuming compartment behind the body compartment. Thus, the brain as energy consumer becomes an indispensable compartment in a systemic metabolism model. Beside the theoretical use of a comprehensible model frame for analyzing the metabolism and its pathologies, we present selected clinical applications where the systemic understanding of the human metabolism directly indicates therapeutic interventions. Future work will deal with the inclusion of the metabolic memory, the stress axis or the sleep rhythm into the integrated model. Conference: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour, 23554 Luebeck, Germany, 27 May - 28 May, 2010. Presentation Type: Oral Presentation Topic: Talks Citation: Langemann D (2010). The supply chain of the brain – An economic approach to human energy metabolism. Front. Neurosci. Conference Abstract: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour. doi: 10.3389/conf.fnins.2010.08.00002 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 12 Apr 2010; Published Online: 12 Apr 2010. * Correspondence: Dirk Langemann, Technische Universität Braunschweig, Institute of Computational Mathematics, Braunschweig, Germany, d.langemann@tu-bs.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Dirk Langemann Google Dirk Langemann Google Scholar Dirk Langemann PubMed Dirk Langemann Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Using a Model of Human Energy Metabolism to Estimate Energy Costs of Turnover

The goal of this research is to use a computational model of nutrient digestion and metabolism in a human to predict energy use and quantify effects of increased futile cycling on energy metabolism. The model is composed of 6 state variables representing amino acids, body protein, visceral protein, glucose, triglyceride, and fatty acids. Differential equations represent carbohydrate, amino acid, and fatty acid uptake and output by tissues. The model estimates metabolizable energy, heat production (HP), respiratory quotient, P/O ratio, energy balance and glucose and fatty acid oxidation based on ATP creation and use, O2 use, CO2 production, heats of combustion, and nutrient flux. Protein deposition is a function of maximum genetic potential for protein accretion. Adipose deposition is a function of energy balance. To examine effects of increasing protein and adipose turnover, protein turnover increased from 2 to 14 %/day and adipose turnover increased from 1.5 to 3.0 %/day for a 70 kg male. Increasing protein turnover increased HP from 11.2 to 20.5 MJ/day, increased glucose oxidation from 1.88 to 2.29 mole/day, increased fatty acid oxidation from 0.132 to 0.873 mole/day and decreased body weight by 6 kg over a 30 day simulation. Increasing adipose turnover decreased HP from 10.8 to 10.7 MJ/day, decreased glucose oxidation from 2.18 to 2.04 mole/day, increased fatty acid oxidation from 0.0200 to 0.0543 mole/day, and decreased body weight by 4.5 kg over a 30 day simulation. Therefore the model is able to predict body weight loss due to increased heat production from increased energy use as a result of changes in muscle and adipose turnover. Since humans are genetically diverse with a range of basal metabolic rates, activity levels and diets, a computational model will quantify diversity and predict metabolic function for a wide range of individuals.

Effects of novel capsinoid treatment on fatness and energy metabolism in humans: possible pharmacogenetic implications

BackgroundCapsinoids from the Capsicum genus of plants are nonpungent capsaicin-related substances with effects on metabolism and body weight in animals. ObjectivesOur objectives were to explore the safety and efficacy of capsinoids taken orally (6 mg/d) for weight loss, fat loss, and change in metabolism and to examine whether candidate genes are predictors of capsinoid response. DesignThis was a 12-wk, placebo-controlled, double-blind, randomized study. Eligibility criteria included a body mass index (BMI; in kg/m2) of 25–35. Body weight was measured, and dual-energy X-ray absorptiometry, indirect calorimetry (men only), and genotyping were conducted. ResultsForty women and 40 men with a mean (± SD) age of 42 ± 8 y and BMI of 30.4 ± 2.4 were randomly assigned to a capsinoid or placebo group. Capsinoids were well tolerated. Mean (± SD) weight change was 0.9 ± 3.1 and 0.5 ± 2.4 kg in the capsinoid and placebo groups, respectively (P = 0.86). There was no significant group difference in total change in adiposity, but abdominal adiposity decreased more (P = 0.049) in the capsinoid group (−1.11 ± 1.83%) than in the placebo group (−0.18 ± 1.94%), and this change correlated with the change in body weight (r = 0.46, P < 0.0001). Changes in resting energy expenditure did not differ significantly between groups, but fat oxidation was higher at the end of the study in the capsinoid group (least-squares mean difference: 21.0 mg/min; P = 0.06). Of 13 genetic variants tested, TRPV1 Val585Ile and UCP2 −866 G/A correlated significantly with change in abdominal adiposity. ConclusionsTreatment with 6 mg/d capsinoids orally appeared to be safe and was associated with abdominal fat loss. Capsinoid ingestion was associated with an increase in fat oxidation that was nearly significant. We identified 2 common genetic variants that may be predictors of therapeutic response.

Effects of 3-Week Consumption of Green Tea Extracts on Whole-Body Metabolism During Cycling Exercise in Endurance-Trained Men

The consumption of green tea has been generally associated with beneficial effects on human whole-body metabolism and recent investigations with animals indicate favorable effects of green tea extracts (GTE) on energy metabolism during exercise and aerobic exercise performance. Therefore, the purpose of this study was to examine the effects of a three-week supplementation with GTE on human energy metabolism during submaximal cycling exercise. In a randomized, double-blind crossover setting, ten healthy endurance-trained men exercised for 2 hours at 50 % W(max) before and after three weeks of placebo or GTE supplementation (GTE containing about 160 mg x day(-1) total catechins, of which about 70 mg x day(-1) was epigallocatechin-3-gallate). The GTE supplementation did not influence indices of fat and energy metabolism (fatty acids, 3-beta-hydroxybutyrate, triacylglycerol, low-density-lipoprotein cholesterol, total cholesterol, lactate, glucose, oxygen uptake, respiratory exchange ratio, energy expenditure), inflammation processes (interleukin-6, C-reactive protein), and oxidative stress (thiobarbituric-acid reactive substances, oxidized low-density-lipoprotein cholesterol), but plasma creatine kinase concentration at rest and during exercise was significantly lower (p = 0.039) and high-density-lipoprotein cholesterol concentration at rest was significantly higher (p = 0.043) compared to placebo. In conclusion, these results suggest only slight effects on whole-body metabolism after supplementation with GTE.

CPEB regulation of human cellular senescence, energy metabolism, and p53 mRNA translation

Cytoplasmic polyadenylation element-binding protein (CPEB) stimulates polyadenylation and translation in germ cells and neurons. Here, we show that CPEB-regulated translation is essential for the senescence of human diploid fibroblasts. Knockdown of CPEB causes skin and lung cells to bypass the M1 crisis stage of senescence; reintroduction of CPEB into the knockdown cells restores a senescence-like phenotype. Knockdown cells that have bypassed senescence undergo little telomere erosion. Surprisingly, knockdown of exogenous CPEB that induced a senescence-like phenotype results in the resumption of cell growth. CPEB knockdown cells have fewer mitochondria than wild-type cells and resemble transformed cells by having reduced respiration and reactive oxygen species (ROS), normal ATP levels, and enhanced rates of glycolysis. p53 mRNA contains cytoplasmic polyadenylation elements in its 3' untranslated region (UTR), which promote polyadenylation. In CPEB knockdown cells, p53 mRNA has an abnormally short poly(A) tail and a reduced translational efficiency, resulting in an approximately 50% decrease in p53 protein levels. An shRNA-directed reduction in p53 protein by about 50% also results in extended cellular life span, reduced respiration and ROS, and increased glycolysis. Together, these results suggest that CPEB controls senescence and bioenergetics in human cells at least in part by modulating p53 mRNA polyadenylation-induced translation.

The Development of Porcine Models of Obesity and the Metabolic Syndrome ,

Despite aggressive research aimed at understanding the myriad biochemical factors that are integrated to balance energy intake and expenditure to maintain normal body weight, obesity is increasing at an alarming rate, and the long-term success of prevention and intervention strategies is minimal. Because much of the scientific literature addressing obesity has originated with rodent models, there is considerable interest among researchers and funding agencies in the development of comparative animal models. Furthermore, numerous disparate results between rodent models and humans (i.e., adipsin, leptin, resistin, tumor necrosis factor-α, and other adipokines) have hindered the translation of rodent data into actionable technologies for humans. The pig is an exceptional restenosis model, and is emerging rapidly as a biomedical model for energy metabolism and obesity in humans because it is devoid of brown fat postnatally and because of their similar metabolic features, cardiovascular systems, and proportional organ sizes. This article highlights the current literature devoted to the development of porcine models for obesity and the metabolic syndrome, with a particular emphasis on the role of adipose tissue and adipokines in the regulation of energy balance and the inflammation associated with obesity.

Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women

An unresolved issue in the field of diet and health is if and how changes in meal frequency affect energy metabolism in humans. We therefore evaluated the influence of reduced meal frequency without a reduction in energy intake on glucose metabolism in normal-weight, healthy male and female subjects. The study was a randomized crossover design, with two 8-week treatment periods (with an intervening 11-week off-diet period) in which subjects consumed all of their calories for weight maintenance distributed in either 3 meals or 1 meal per day (consumed between 4:00 pm and 8:00 pm). Energy metabolism was evaluated at designated time points throughout the study by performing morning oral glucose tolerance tests and measuring levels of glucose, insulin, glucagon, leptin, ghrelin, adiponectin, resistin, and brain-derived neurotrophic factor (BDNF). Subjects consuming 1 meal per day exhibited higher morning fasting plasma glucose levels, greater and more sustained elevations of plasma glucose concentrations, and a delayed insulin response in the oral glucose tolerance test compared with subjects consuming 3 meals per day. Levels of ghrelin were elevated in response to the 1-meal-per-day regimen. Fasting levels of insulin, leptin, ghrelin, adiponectin, resistin, and BDNF were not significantly affected by meal frequency. Subjects consuming a single large daily meal exhibit elevated fasting glucose levels and impaired morning glucose tolerance associated with a delayed insulin response during a 2-month diet period compared with those consuming 3 meals per day. The impaired glucose tolerance was reversible and was not associated with alterations in the levels of adipokines or BDNF.

Lessons from “Lower” Organisms: What Worms, Flies, and Zebrafish Can Teach Us about Human Energy Metabolism

A pandemic of metabolic diseases (atherosclerosis, diabetes mellitus, and obesity), unleashed by multiple social and economic factors beyond the control of most individuals, threatens to diminish human life span for the first time in the modern era. Given the redundancy and inherent complexity of processes regulating the uptake, transport, catabolism, and synthesis of nutrients, magic bullets to target these diseases will be hard to find. Recent studies using the worm Caenorhabditis elegans, the fly Drosophila melanogaster, and the zebrafish Danio rerio indicate that these “lower” metazoans possess unique attributes that should help in identifying, investigating, and even validating new pharmaceutical targets for these diseases. We summarize findings in these organisms that shed light on highly conserved pathways of energy homeostasis.

Gain-of-Function R225W Mutation in Human AMPKγ3 Causing Increased Glycogen and Decreased Triglyceride in Skeletal Muscle

BackgroundAMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that is evolutionarily conserved from yeast to mammals and functions to maintain cellular and whole body energy homeostasis. Studies in experimental animals demonstrate that activation of AMPK in skeletal muscle protects against insulin resistance, type 2 diabetes and obesity. The regulatory γ3 subunit of AMPK is expressed exclusively in skeletal muscle; however, its importance in controlling overall AMPK activity is unknown. While evidence is emerging that gamma subunit mutations interfere specifically with AMP activation, there remains some controversy regarding the impact of gamma subunit mutations [1]–[3]. Here we report the first gain-of-function mutation in the muscle-specific regulatory γ3 subunit in humans.Methods and FindingsWe sequenced the exons and splice junctions of the AMPK γ3 gene (PRKAG3) in 761 obese and 759 lean individuals, identifying 87 sequence variants including a novel R225W mutation in subjects from two unrelated families. The γ3 R225W mutation is homologous in location to the γ2R302Q mutation in patients with Wolf-Parkinson-White syndrome and to the γ3R225Q mutation originally linked to an increase in muscle glycogen content in purebred Hampshire Rendement Napole (RN-) pigs. We demonstrate in differentiated muscle satellite cells obtained from the vastus lateralis of R225W carriers that the mutation is associated with an approximate doubling of both basal and AMP-activated AMPK activities. Moreover, subjects bearing the R225W mutation exhibit a ∼90% increase of skeletal muscle glycogen content and a ∼30% decrease in intramuscular triglyceride (IMTG).ConclusionsWe have identified for the first time a mutation in the skeletal muscle-specific regulatory γ3 subunit of AMPK in humans. The γ3R225W mutation has significant functional effects as demonstrated by increases in basal and AMP-activated AMPK activities, increased muscle glycogen and decreased IMTG. Overall, these findings are consistent with an important regulatory role for AMPK γ3 in human muscle energy metabolism.

Energy Metabolism During Human Pregnancy

This review summarizes information regarding how human energy metabolism is affected by pregnancy, and current estimates of energy requirements during pregnancy are presented. Such estimates can be calculated using either increases in basal metabolic rate (BMR) or increases in total energy expenditure (TEE). The two modes of calculation give similar results for a complete pregnancy but different distributions of energy requirements in the three trimesters. Recent information is presented regarding the effect of pregnancy on BMR, TEE, diet-induced thermogenesis, and physical activity. The validity of energy intake (EI) data recently assessed in well-nourished pregnant women was evaluated using information regarding energy metabolism during pregnancy. The results show that underreporting of EI is common during pregnancy and indicate that additional longitudinal studies, taking the total energy budget during pregnancy into account, are needed to satisfactorily define energy requirements during the three trimesters of gestation.

The energetics of human walking: Is Froude number ( Fr) useful for metabolic comparisons?

Velocity and body mass have well-known influences on the amount of metabolic energy that animals require to walk. This relationship could stem from the fact that both are key variables in calculating the mechanical energy of a system in motion. Other variables, like leg length, are also important in mechanical energy calculations and two mechanical formulations that incorporate leg length, Froude number ( Fr) and the LiMb model, have been shown to correlate with human metabolic energy expenditure. Both, however, include velocity as a key variable in their calculations, so we wondered if the correlation might derive solely from their relationship with velocity rather than leg length. Using the energetic data and gait parameters from 24 human adults and 48 children, we tested several variables – velocity ( V), V 2, body mass, leg length, Fr and LiMb – to see which combinations best explained the variation in oxygen consumption, a proxy of metabolic energy expenditure. An equation with V 2, body mass and leg length as covariates produced the highest R 2, explaining 88% of the variation when all subjects were combined. No significant differences in the predictive power of velocity, V 2, Fr or LiMb were detected, prompting us to conclude that neither Fr nor LiMb compensate for the effect of leg length. Leg length does influence the energetic expenditure of walking humans, but Fr and LiMb do not appear to adequately reflect that effect. The development of another method to compensate for the effect of leg length on metabolic energy consumption is essential.

Identifying important measurements to describe human energy metabolism

Experimental measurements at the cellular and tissue level that are critical to understanding energy metabolism can be difficult to identify. To that end, a computer model of human energy metabolis...

Effect of a Thermogenic Beverage on 24‐Hour Energy Metabolism in Humans

To test whether consumption of a beverage containing active ingredients will increase 24-hour energy metabolism in healthy, young, lean individuals. Thirty-one male and female subjects consumed 3 x 250-mL servings of a beverage containing green tea catechins, caffeine, and calcium for 3 days in a single-center, double-blind, placebo-controlled, cross-over design study. On the 3rd day, 23-hour energy metabolism, extrapolated to 24-hour, was measured in a calorimeter chamber. Blood pressure and heart rate were measured, and total day and night urines were analyzed for urea and catecholamine excretion. Twenty-four-hour energy expenditure (EE) and 24-hour fat oxidation were lower in women than in men (p < 0.0001 and p < 0.015, respectively). Although there were no treatment or treatment/gender effects on substrate oxidation, treatment increased 24-hour EE by 106 +/- 31 kcal/24 hours (p = 0.002), equivalent to 4.7 +/- 1.6 kcal/h (day; p = 0.005) and 3.3 +/- 1.5 kcal/h (night; p = 0.04). No significant differences were observed in hemodynamic parameters. The present study provides evidence that consumption of a beverage containing green tea catechins, caffeine, and calcium increases 24-hour EE by 4.6%, but the contribution of the individual ingredients cannot be distinguished. Although this increase is modest, the results are discussed in relation to proposed public health goals, indicating that such modifications are sufficient to prevent weight gain. When consumed regularly as part of a healthy diet and exercise regime, such a beverage may provide benefits for weight control.

Health Promotion and Genome in Japanese

Current health promotion is based on average evaluations obtained from statistics of large populations but, in reality, the range of 2SD (standard deviation) may not cover medical and nutritional requirements owing to genetic polymorphisms among healthy individuals. Thus, nutrigenomics in human energy metabolism is needed for personalized health promotion based on individual genetic evaluation of single nucleotide polymorphisms (SNPs) etc. Energy metabolism depends on thrifty genes including SNPs of transporters (uncoupling proteins etc.) and receptors (adrenergic receptors etc.) . The impact of Westernization on both nutrition and thrifty genes of Japanese has caused a rapid increase in metabolic syndrome. In health promotion, personality is also important in behavioral change; most Japanese have the obedient S/S genotype of the serotonin transporter gene, and careful instruction is needed in health promotion. Our personalized health promotion program reversed metabolic syndrome, not only in the short-term (11 months), but also in the long-term (average, 23 years) irrespective of the presence of thrifty genes. However, the rapid increase in metabolic syndrome will need more advanced omics of adipose tissue, including those of prohibitin and resveratrol. The prevention of final disability resulting from cardiovascular diseases and dementia is important. In addition to thrifty genes, we should consider methylene tetrahydrofolate reductase SNP in C677T. To prevent hyperhomocysteinemia, improvement of serum folate was easier when genome information was given to examinees.

Distribution of ghrelin-immunoreactive neuronal networks in the human hypothalamus

Ghrelin has been discovered as the endogenous ligand of the growth hormone secretagogue receptor (GHS-R). It stimulates growth hormone secretion and also potently increases food intake. To date, ghrelin is the only known peripheral orexigenic hormone. Recent studies have demonstrated that in addition to peripheral organs, ghrelin is also synthesized in the hypothalamus. In the present study, we examined the distribution of the ghrelin-immunoreactive (IR) elements in the human hypothalamus. Ghrelin-IR fibers were widely distributed throughout the hypothalamus. Based on the thickness of fibers, major subtypes of ghrelin-IR axons were observed: thick fibers with large varicosities and very fine axons with or without small varicosities. Dense networks of ghrelin-IR axons were observed in the hypothalamic suprachiasmatic, paraventricular, supraoptic, dorsomedial, ventromedial and infundibular nuclei and in the periventricular area. Ghrelin-IR axons also appeared in the external layer of the pituitary stalk. Ghrelin-IR cell bodies were not detected. Since hypothalamic regions innervated by ghrelin-IR axons also take part in the regulation of food intake and energy balance, the centrally synthesized ghrelin may play a major role in the central regulation of energy metabolism in humans.

In vivo effects of corticotropin-releasing hormone on femoral adipose tissue metabolism in women

To investigate whether i.v. injected corticotropin-releasing hormone (CRH) (1 microg/kg) has a direct effect on adipose tissue metabolism in humans. Double-blinded, placebo-controlled, crossover study. Twelve healthy normal weight female volunteers (age 20-37 years, body mass index: 22.75+/-1.33 kg/m(2)) Assessment of local generation of glycerol, and glucose in adipose tissue by microdialysis. Measurement of adipose tissue and skin blood flow by laser Doppler flowmetry. Injection of CRH acutely increases interstitial concentrations of glycerol (19.0+/-5.4%, P<0.05) and glucose (13.5+/-5.8%, P<0.05) reaching peak levels after 15 min. Plasma glycerol increases in parallel (Delta=16.7+/-5.9% after 15 min (P<0.05)), whereas plasma glucose remains unaffected. Changes in tissue blood flow do not explain interstitial metabolite alterations. Initial CRH effects on adipose tissue metabolism are short lasting and disappear after 15 min. The importance of CRH on human energy metabolism is underlined by the present in vivo study demonstrating peptidergic effects on lipolysis and glucose homeostasis in human subcutaneous adipose tissue.

Age-related changes in human skeletal muscle mitochondrial energy metabolism

Age-related changes in human skeletal muscle mitochondrial energy metabolism